VASODILATATION PRODUCED BY STIMULATION OF PARVOCELLULAR RETICULAR-FORMATION IN THE MEDULLA OF ANESTHETIZED-DECEREBRATE CATS

In cats activation of the dorsal facial area (DFA) in the medulla prod uced an increase of blood flow in the common carotid artery (CCA). Thi s involves flow increases in both intra-and extra-cranial vessels via cranial parasympathetic nerves. In this study, we attempted to explore transmitter mechanisms involved in vasodilatation in extracranial vas cular beds due to DFA activation. Cats were anesthetized with intraper itoneal urethane (350 mg/kg) and chloralose (35 mg/kg). Electrical sti mulation (100 mu A, 20 Hz, 0.5 ms for 5 s) or microinjection of sodium glutamate (Glu, 0.25 M(i) 50 nl) in DFA increased the. velocity of fl ow in CCA ipsilateral to the stimulation. After control values were ob tained, the animals were, subjected to decerebration with transection level just rostral to superior colliculi (precollicular decerebration) . The increased CCA flow velocity induced by DFA activation was not al tered before and after decerebration. Atropine (muscarinic blocker, 0. 5-2.0 mg/kg, i.v.) alone only partially attenuated the increase, but t he increase was totally blocked by additional N-omega-L-arginine methy l ester (nitric oxide synthase inhibitor) in 7 out of 9 cats. These fi ndings suggest that extracranial vasodilatation induced by DFA activat ion does not depend on the sympathetic nervous system, but involves th e muscarinic- and nitric-oxide-mediated systems.